L17 Respiratory Failure

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jknell
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200624
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L17 Respiratory Failure
Updated:
2013-02-17 13:53:26
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Pulmonary II
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Pulmonary II
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  1. Normal Ventilation
    -V and Q are matched due to hypoxic vasoconstriction

    • Under normal physiologic conditions (pH):
    • -minute ventilation varies to target PCO2 of 40 

    • Under abnormal conditions (abnormal pH):
    • -minute ventilation varies to target a normal pH (pH trumps CO2 for respiratory drive)
    • -metabolic acidosis → ↑ ventilation until pH >7.35
    • -metabolic alkalosis → inhibit ventilation until pH <7.45 

    • Acute Respiratory Acidosis:
    • -pH <7.35
    • -increased PCO2 (relative to their normal) (hypercabic)
  2. Normal Oxygenation
    -PaO2 on 100% FiO2 is ~ 660 mmHg under ideal conditions

    -if PaO2 on 100% FiO2 is < 200 mmHg SHUNT is present

    • Hypoxemic Respiratory Failure = PaO2 < 60 mmHg
    • -end organs are vulnerable to regional hypoxic injury
    • -triggers hyperventilation reflex
  3. A-a Gradient
    -Tells you if there is derangement in oxygenation

    • -Gradient = [(760 - 47 xFiO2) -(pCO2/0.8)] -(PaO2)
    • -Normal gradient should ~ (age/4) + 4

    -Hypoventilation is the only cause of hypoxemia without A-a gradient
  4. Acute Respiratory Failure
    -inability of the respiratory system to maintain adequate gas exchange

    • -arterial PO2 < 60 mmHg
    • OR
    • -PCO2 > 50 mmHg

    In patients with preexisting lung disease these numbers may be normal, therefore, acute respiratory failure is a significant change from the patient's baseline gase exchange status

    **pH can help distinguish if the CO2 retention is acute or chronic
  5. Categories of Acute Respiratory Failure
    • 1. Hypoxemic (with normal or low PCO2): PaO2 < 60 mmHg
    • -pt NOT displaying signs of respiratory distress
    • -mainly occurs due to shunt physiology

    • 2. Hypercapnic/hypercarbic: pH <7.35 with ↑ pCO2
    • -pt working hard to breath
    • -most common cause of respiratory arrest

    • 3. Failure to protect or maintain airway patency
    • -Central: decreased mental status; at risk for airway obstruction
    • -Anatomical narrowing of the airway → stridor
  6. Hypoxemic Acute Respiratory Failure
    • -Acute drop in PaO2 < 60
    • -PCO2 normal or even low

    • Causes: Sudden decrease or absent ventilation to an area with preserved perfusion
    • 1. Pneumonia (localized diseases of the pulmonary parenchyma)
    • 2. ARDS (increase of fluid within alveolar spaces)

    • Symptoms:
    • -confusion, agitation WITHOUT dramatic dyspnea
    • -tachycardia

    • Common Causes (Lecture):
    • -Pneumonia (often intubate)
    • -Bronchospasm - (tx: steroids, beta agonists)
    • -Cardiogenic Pulmonary Edema (rarely have to intubate)
    • -Gastric Aspiration (large volume aspiration)
    • -Non-cardiogenic pulmonary edema
    • -PE

    • Tx:
    • -V/Q mismatch: responds to increased FiO2
    • -Shunt (V=0): poor response to increased FiO2
  7. Hypercapnic/Hypercarbic Acute Respiratory Failure
    • Lecture: pH <7.35 and elevated PCO2 (relative to pH)
    • -pH becomes driving force for ventilation
    • -metabolic acidosis with pH 7.26 should drive ventilation to a PCO2 ~26

    • -PCO2 > 50 mmHg
    • **pH < 7.35 (to show absent/incomplete metabolic compensation)
    • -decreased PaO2 (due to hypoventilation and sometimes V/Q mismatch)

    • Causes: Inadequate ventilation = inadequate CO2 removal
    • 1. Depression of CNS ventilatory control
    • 2. Disease of respiratory bellows (chest wall/neuromuscular)
    • 3. Chronic obstructive lung disease

    *patients often have preexisting disease that makes them more vulnerable to an acute problem --> acute on chronic respiratory failure

    • Symptoms:
    • -Acidosis: dramatic dyspnea, increased work of breathing
    • -progressive decrease in pH causes loss of vascular tone (hypotension, tachyarrhythmia)
    • -Narcosis: ↑PCO2 → obtundation
  8. General Symptoms of Acute Respiratory Failure
    • 1. Dyspnea
    • 2. Impaired mental status
    • 3. HA (hypercapnia)
    • 4. Tachycardia
    • 5. Papilledema (hypercapnia --> cerebral vessel dilation)
    • 6. Lung findings depend on underlying disease
    • 7. Cyanosis (severe hypoxemia)
  9. Hypoxemic Respiratory Failure: Gas Exchange Abnormality
    • Causes of Hypoxemia
    • 1. VQ Mismatch
    • -Ventilation in some regions limited
    • -Prefusion normal
    • *responds to 100% O2

    • 2. Shunt
    • -Ventilation is completely absent
    • -Perfusion normal
    • *does NOT respond to 100% O2

    **CO2 eliminate is normally adequate b/c patients are able to maintain alveolar ventilation (compensate by increasing minute ventilation)
  10. Chronic Hypoxemic Respiratory Failure
    • -gradual drop in PaO2 <60 (typically >55)
    • Causes:
    • -heterogenous lung disease
    • -VQ mismatch (typically obstructive)
    • -hypoventilation

    • Symptoms:
    • -mild cognitive impairement
    • -exercise limited by ventilation

    -tx with O2 to prevent cardiac complications and risk of sudden death (not exercise intolerance)
  11. Treatment of Acute Hypoxemic Respiratory Failure
    • OPTIMIZE O2 TRANSPORT TO TISSUES:
    • 1. Arterial O2 Saturation
    • -Target O2 Sat >90% (PO2 >60 without hypocarbia)
    • *lecture says >95% (buffer zone in case pt isn't on the 'normal' dissociation curve)
    • *may need to intubate if can't achieve PO2 >60
    • 2. Acceptable Hg level
    • -Target > 10 g/dL
    • 3. Normal-near normal Cardiac Output
    • 4. PEEP for ARDS

    • MAINTAIN CO2 ELIMINATION:
    • -maintain an acceptable pH rather than a normal PCO2
    • -may need to ventilate if PaCO2 rises enough to cause pH < 7.3 or impaired mental status

    • REDUCE WORK OF BREATHING:
    • -mechanical ventilation
    • -rests respiratory muscles
  12. Treatment: Arterial O2 Saturation
    • -Hb is approximately 90% saturated at PO2 of 60
    • -PO2 much beyond this point does not provide much benefit
    • -"margin of safety": maintain PO2 of 65 where Hb is 95% saturated and pH will remain normal (if not can get an ABG to check pH)

    • Patients at risk for hypoxic respiratory arrest get 100% FiO2:
    • -extreme V/Q mismatch
    • -hypoxemia despite O2 4-6 L/min
    • **may lead to increased CO2 (~6mmHg) retention in COPD patients but avoiding hypoxic respiratory arrest is more important!
  13. Treatment: CO2 retention with high FiO2 (Blue Bloater)
    • -in patients with chronic hypercapnia (due to underling lung disease) supplemental O2 may further increase PCO2
    • -NOT due to inhibition of drive
    • -due to inhibition of hypoxic vasoconstriction --> ventilation of relatively unperfused units(????????????? seems to show perfusion of relatively unventilated regions)
    • -of little clinical significance
  14. Treatment: CO2 retention with high FiO2 (Pink Puffer)


    • Pink Puffers will increase their respiratory rate to reduce the amount of CO2 retained

    They will complain of dyspnea but won't retain more CO2 and develop acidosis
  15. Hypercapnic/Hypoxemic Respiratory Failure: Gas Exchange Abnormalities
    • MECHANISMS OF HYPERCAPNIA:
    • -patients are unable to maintain a level of alveolar ventilation sufficient to eliminate CO2

    • Mechanisms of Insufficient Ventilation:
    • 1. decreased minute ventilation
    • 2. decreased effectiveness of ventilation (increased VD/VT)

    VD/VT: relative amount of alveolar vs dead space ventilation (increased dead space)

    • Stages Affected:
    • 1. Respiratory Generator in the CNS
    • -Drugs
    • -hypothyroidism
    • -metabolic alkalosi
    • -structural lesions

    • 2. Chest wall/Neuromuscular system
    • -Kyphoscoliosis
    • -Myasthenia Gravis
    • -Guillian Barre
    • -ALS
    • -Polymyositis
    • -Cervical cord injury
    • -obesity
    • -electrolyte abnormalities

    • 3. Lungs/Airways
    • -COPD
    • -LVF
    • -Severe ARDS
    • -Severe Asthma

    • MECHANISMS OF HYPOXEMIA:
    • 1. Hypoventilation
    • 2. V/Q mismatch

    • **rarely see shunt --> most respond to 100% O2
    • **BUT O2 can lead to a further increase in PaCO2!!!!

    • Patients who are acidotic have dramatic sx (dyspnea, hypotension, tachyarrhythmia)
  16. Physiologic Effects of Acute Hypercarbia
    • 1. CO2 Narcosis
    • -sleepy to obtundation

    • 2. Acidosis
    • -dyspnea
    • -hypotension
    • -tachyarrhythmias
    • -PEA arrest if pH < 7.15
  17. Chronic Hypercarbic Failure
    • 1. Obstructive lung diseases (most common)
    • 2. Restrictive lung diseases (late in fibrosis)
    • 3. Hypoventilation syndromes

    Patients are typically dyspneic with an increased work of breathing
  18. Acute on Chronic Respiratory Failure
    • Causes:
    • 1. Acute respiratory tract infection (usually viral)
    • 2. Drugs that suppress the respiratory center (sedatives, narcotics)
    • 3. CHF
    • 4. Less Common: PE, environmental pollutants
  19. Blue Bloater
    • Normal:
    • -Elevated PaCO2
    • -slight respiratory acidosis

    • COPD Exacerbation:
    • -increase RR
    • -use accessory muscles
    • -increase PaCO2
    • -worsen respiratory acidosis

    • COPD Exacerbation:
    • -can no longer maintain RR --> 8
    • -PaCO2 significantly increases
    • -severe acute respiratory acidosis
    • -obtundation (CO2 narcosis)
  20. Pink Puffer
    • COPD:
    • -increased RR (22)
    • -pH normal
    • -PaCO2 only slightly elevated

    • COPD Exacerbation:
    • -increase RR (26)
    • -use of accessory muscles
    • -PaCO2?? (should decrease)
    • -pH decrease

    • COPD Exacerbation:
    • -can no longer maintain RR --> 8
    • -breathing is shallow and ineffective
    • -PaCO2 significantly increases
    • -acute respiratory acidosis
    • -CO2 Narcosis (PaCO2 much less than BB --> obtundation is a relative phenomenon)
  21. Acute Hypercarbic Respiratory Failure (without chronic lung disease)
    • Normal Patient: ie Diabetic

    • Metabolic Acidosis (DKA)
    • -hyperventilation (RR 30)
    • -PaCO2 decreases
    • -pH decreases
    • ***want to intubate here

    • -hyperventilation (RR40)
    • -accessory muscle use
    • -further decrease in PaCO2
    • -further decrease in pH
    • ***Don't intubate here! Can't move as much air as they can

    • -Hyperventilation (RR 45)
    • -shallow and ineffective
    • -acute respiratory acidosis
    • -slight increase in PaCO2
    • -pH decreases

    • PEA arrest from acidosis
    • -PaCO2 never went over 40!
  22. Treatment: Acute Hypercapnic Respiratory Failure
    1. BiPAP (only CI: altered mental status or secretions)

    2. Tx underlying cause
  23. Failure to protect or maintain airway patency
    • 1. Central
    • -commonly from respiratory depressants
    • -obtunded
    • -at risk for gastric aspiration, oral aspiration, mucus plugging

    • 2. Airway Obstruction (anatomic narrowing)
    • -extreme dyspnea
    • -anxiety
    • -increased work of breathing
    • -stridor if obstruction is extrathoracic
  24. Central Hypercarbic Failure (Abnormal Drive)
    • 1. CNS Depression
    • -drugs
    • -encephalopathy

    • 2. Intrinsic decreased sensitivity to CO2
    • -obesity hypoventilation
    • -myxedema coma

    • 3. CNS Disease
    • -brain stem tumors

    Often detected as an O2 desat in sleeping patient

    • Symptoms:
    • -minimal dyspnea
    • -normal to diminished respiratory effort
    • -sleep to obtunded mental status

    • Treatment:
    • -tx underlying condition
    • -must protect airway: DO NOT USE BiPAP
    • -Intubation
  25. Anatomical Airway Patency Failure
    • 1. Allergic reaction
    • 2. Postop swelling
    • 3. Oropharyngeal abscess
    • 4. Viral infection

    • Treatment:
    • -intubation can be difficult due to swelling (preemptive intubation)
  26. Mixed Hypercarbic Failure
    • -any combination of parenchymal disease, acid load and drive
    • -COPD + Bowel Ischemia
    • -COPD + Bowel Ischemia + Narcotics for abdominal pain

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